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Equine Protozoal Myeloencephalitis (view source)
Revision as of 11:25, 21 July 2010
, 11:25, 21 July 2010→Life Cycle
[[Image:Equine_Protozoal_Myeloencephalitis_life_cycle.jpg|600px|thumb|centre|''' Life cycle diagram of ''Sarcocystis neurona''. Created by the ''Agricultural Research Service, the research agency of the United States Department of Agriculture'', July 2005. ''Sourced from the USDA Agricultural Research Service page on EPM/Sarcocystis neurona, located via WikiMedia Commons.'' ''']]
[[Image:Equine_Protozoal_Myeloencephalitis_life_cycle.jpg|600px|thumb|centre|''' Life cycle diagram of ''Sarcocystis neurona''. Created by the ''Agricultural Research Service, the research agency of the United States Department of Agriculture'', July 2005. ''Sourced from the USDA Agricultural Research Service page on EPM/Sarcocystis neurona, located via WikiMedia Commons.'' ''']]
See [[Sarcocystis|here]] for further details of the life cycle of ''Sarcocystis neurona''.
Infective sporocysts are passed in the faeces of the definitive host and must be ingested by the horse for infection to occur.(Furr) See [[Sarcocystis|here]] for further details of the life cycle of ''Sarcocystis neurona''.
The causative pathogen(s) have been isolated from species other than the horse including zebra, domestic cat, Canadian lynx, sea otter, straw-necked ibis, mink, raccoon and sunk. (Furr)
The causative pathogen(s) have been isolated from species other than the horse including zebra, domestic cat, Canadian lynx, sea otter, straw-necked ibis, mink, raccoon and sunk. (Furr)
==Pathogenesis==
Immune clearance of the organsim must be, in the large part, very effective, since less than 1% of horses exposed to the protozoan suffer from EPM.(24 in Furr) Factors which promote disease develpoment include parasite dose (71 in Furr) and probably virulnece of the protozoal strain. Stress induced by preganancy, travel, training, showing (25 in Furr) may have an immunosuppressive effect that encourages infection. Indeed, it has been shown that stress affctes the severity of clincal sigsn seen in natural infections (74 in Furr)
The 'Trojan horse' hypothesis suggests that S.neurona meroziotes traverse the blood brain barrier encrypted within leucocytes that have pahgocytosed the parasite in the periphery. Subsequent eggression and infection of other cells once inside the CNS, results in encephalitis.<ref>Lindsay, D.S, Mitchell, S.M, Yang, J, Dubey, J.P, Gogal, R.M, Jr, Witonsky, S.G (2006) Penetration of equine leukocytes by merozoites of ''Sarcocystis neurona''. ''Vet Parasitol'', 15:138(3-4):371-6</ref> Other theories include haematogenous spread or direct passage of parasites via the cytoplasm of endothelial cells into the CNS. However, despite extensive histological lesions, few organisms are typically visible in the neural tissues of affected horses. This implies that cytokines and/or metabolites may have a considerable roel in porducign pathological changes.(EPM 6) Althugh the protozoan may iduce some degree of immunosuppression in the host<ref>Spencer, J.A, Ellison, S.E, Guarino, A.J, Blagburn, B.L (2004) Cell-mediated immune responses in horses with equine protozoal myeloencephalitis. ''J Parasitol'', 90(2):428-30.</ref><ref>Yang, J, Ellison, S, Gogal, R, Norton, H, Lindsay, D.S, Andrews, F, Ward, D, Witonsky, S (2006) Immune response to Sarcocystis neurona infection in naturally infected horses with equine protozoal myeloencephalitis. ''Vet Parasitol'', 138(3-4):200-10.</ref>, it is likely that the immune-priveglie of the CNS prevents parasite clearance form this site (Furr). Placental trasnmission is conseiderd highly unlikely (Furr).
Both humoral and cell-mediated immune mechansism are likely to be significant in the host defecne agaisnt ''S.neurona''. Antibodies are porduced soon after infection and offer some degree of protection (furr). CD8 postivie T-cells and their production of IFN-gamma are likely to be pivtoal in the removal of intracellualr stages of the parasite (Furr).
==Signalment==
==Signalment==